“Evolutionary” multiverse theories are a poor explanation for our existence

Argues biologist Austin L. Hughes:

If I toss a coin, it is certain that I will get heads or tails, but that outcome depends on my tossing the coin, which I may not necessarily do. Likewise, any particular universe may follow from the existence of a multiverse, but the existence of the multiverse remains to be explained. In particular, the universe-generating process assumed by some multiverse theories is itself contingent because it depends on the action of laws assumed by the theory. The latter might be called meta-laws, since they form the basis for the origin of the individual universes, each with its own individual set of laws. So what determines the meta-laws? Either we must introduce meta-meta-laws, and so on in infinite regression, or we must hold that the meta-laws themselves are necessary — and so we have in effect just changed our understanding of what the fundamental universe is to one that contains many universes. In that case, we are still left without ultimate explanations as to why that universe exists or has the characteristics it does.

It is possible to be a naturalist without embracing scientism, but it does take some work.


Why does HIV infect T-cells with too many viruses?

Komarova NL, Levy DN, Wodarz D (2012) Effect of Synaptic Transmission on Viral Fitness in HIV Infection. PLoS ONE 7(11): e48361. doi:10.1371/journal.pone.0048361

We have two kidneys, mayflies lay packets of thousands of eggs, and duplicate genes abound in all living things. Gallifreyans even have two hearts. Redundancy is a universal fact of biology — but how does it play a role in HIV?

For HIV infection to grow within a person, it must spread from one T-cell to another. Typically, individual virus particles bud from an infected cell, diffuse through the lymph, and then enter a second T-cell. It just takes a single virus to infect that second cell — and so the many viruses exiting from one cell can infect many other cells. This mode is called cell-free transmission. But there is a second way that T-cell infection can occur: An infected T-cell can “link up” to an uninfected T-cell, forming a synapse between the two. Tens or hundreds of virus particles may then shuttle directly through the synapse, infecting the new cell. This second mode of transmission is called synaptic transmission or direct cell-to-cell transmission.

Why should doctors & patients care? It turns out that this mode of transmission may give the virus a way to avoid the effects of drug treatment. My back-of-the-envelope calculation suggests that synaptic transmission can halve or quarter a patient’s effective drug dose!

But why the virus evolved to spread in this manner is a bit of a puzzle — if only a single particle is needed to infect a cell, why waste hundreds all at once? Does the virus benefit from this alternate lifecycle, or is this redundant mode of transmission a quirky side-effect (a “spandrel”) of T-cell physiology that is just wasteful, from the virus’ perspective?

In PLoS ONE last month, Komarova, Levy, and Wodarz investigate exactly this question by modeling how the virus can evolve to maximize growth of the infection. Using a model of immune response, they conclude that there is room for two opposing viral strategies: a “stealth” strategy where just one or a few viruses infect each cell, and a “saturation” strategy where many viruses infect each cell, ganging up to overwhelm the person’s immune response. Synaptic transmission may have evolved to let HIV “gang up” on the intracellular immune response.

This saturation strategy is analogous to the commonly observed adaptation known as predator satiation — a strategy used by prey species (such as the mayfly laying thousands of eggs!) to flood their immediate environment with many more offspring than the cohabiting predator species can possibly consume. KLW’s model shows a way in which viral saturation can likewise be adaptive.

While they do not say so explicitly, an extension of KLW’s model might also explain the coexistence of cell-free and synaptic modes of transmission, as a way for the virus to “bet hedge” — using the cell-free mode to spread quickly in permissive immune environments, and using the synaptic mode to ensure safe passage from cell to cell when confronted with a stronger immune response. Even with the uncertainty surrounding exactly how to model the immune response, KLW’s theory should provide a helpful framework for virologists who want to think about the evolutionary causes and pathological effects of synaptic transmission.

Hello World!

I woke up the other day and said to myself,

“You’re a mathematical biologist, and you’re doing pretty cool stuff, but there’s an entire world of mathy-bio types doing amazing things… and you know so little about them!  You’ve read such a tiny fraction of the literature out there — so what do you know?”

This blog is my attempt to push myself to read a slightly larger fraction of what’s out there, to think about it, to write about it, and — if my dear readers are so inclined — to have conversations about it. Welcome to all!